Cited by 74Diet, Metabolism, and DiseaseDiabetes Treatment and ManagementRegulation of Appetite and Obesity

High glycemic index metabolic damage – a pivotal role of GIP and GLP-1

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Pfeiffer, Andreas F.H., Keyhani-Nejad, Farnaz·2018·Trends in Endocrinology & Metabolism

Abstract

When glucose-fructose dimers are supplied as the slowly digestible, completely absorbable, low glycemic index (GI) sugar isomaltulose, the detrimental effects of high GI sucrose are avoided. This difference requires the presence of intact glucose-induced insulinotropic peptide receptor (GIPR) and is mediated by the rapid uptake of glucose and the stimulation of GIP release from K cells in the upper small intestine. GIP promotes lipogenesis, fatty liver, insulin resistance, and postprandial inflammation, and reduces fat oxidation in skeletal muscle, partly by hypothalamic interference with energy partitioning and epigenetic programming. GIP is similarly required for the detrimental metabolic effects of other high GI carbohydrates. We therefore propose that the release of GIP in the upper small intestine is an important determinant of the metabolic quality of carbohydrates.

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Crossref · 10.1016/j.tem.2018.03.003

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Authors
Pfeiffer, A. F. H., & Keyhani-Nejad, F.
Affiliations
German Center for Diabetes Research (DE)
Corresponding author
Pfeiffer, Andreas F.H.
Venue
Trends in Endocrinology & Metabolism
Publisher
Elsevier BV
Published
2018-05
Volume
29
Issue
5
Pages
289-299
ISSN
1043-2760 (ISSN-L)
OpenAlex
W2795231384
Cited by
74
References
65
Citations by year
2026: 4 · 2025: 7 · 2024: 10 · 2023: 7 · 2022: 12 · 2021: 11 · 2020: 6 · 2019: 16 · 2018: 1
FWCI
1.31
Type
journal article
Language
en
Open access
Locations
  • Trends in Endocrinology and Metabolism (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Keywords
glycemic index, isomaltulose, glucagon-like peptide-1, GIP receptor, K cells, sucrose, lipogenesis, hepatic steatosis, insulin resistance, postprandial inflammation, fat oxidation, energy allocation, epigenetic programming, carbohydrate metabolism
MeSH terms
Animals, Gastric Inhibitory Polypeptide, Humans, Inflammation, Insulin, Muscle, Skeletal, Postprandial Period, Glycemic Index, Glucagon-Like Peptide 1, Incretins

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